Men, women, and children experience alopecia, the clinical term for hair loss. Androgenetic alopecia or pattern baldness, which is believed to result from a combination of genetic and hormonal causes, is by far the most common form of hair loss. It is the largest single type of recognizable alopecia to affect both men and women. The rate of hair shedding in androgenetic alopecia is affected by three forces: advancing age, an inherited tendency to bald early, and an over-abundance of the male hormone dihydrotestosterone (DHT) within the hair follicle. DHT is a highly active form of testosterone, which influences many aspects of behavior, from sex drive to aggression. The conversion from testosterone to DHT is driven by an enzyme called 5-alpha reductase, which is produced in the prostate, various adrenal glands, and the scalp. Over time, the action of DHT causes the hair follicle to degrade and shortens the anagen phase. Some follicles will gradually die, but most will simply shrink in size and produce weaker hairs. With a steadily shorter anagen growing cycle, more hairs are shed because the hairs becoming thinner and thinner until they are too fine to survive daily wear and tear. Balding hair gradually changes from long, thick, coarse, pigmented hair into fine, unpigmented vellus sprouts.
There is much debate on the mechanism that causes the hormonal degradation of the hair follicle, but it has been hypothesized that the hormone triggers an autoimmune response that initiates an attack on the hair follicle, resulting in destructive inflammation. It may be that androgens somehow alter the follicle, causing it to be labeled as a foreign body. The follicles then gradually wither under the onslaught of the attack. Another possible complementary explanation is that androgens also trigger increased sebum production, which favors an excessive microbial population that leads to the same inflammatory autoimmune response. In any case, hair progressively miniaturizes under the autoimmune attack, so that with each growth cycle it gets shorter and thinner until it finally turns into tiny unpigmented vellus hair.
Pattern hair loss appears to have other causes as well. For instance, damage to blood vessel linings can inhibit a growth factor they ordinarily produce: endothelium-derived relaxing factor (EDRF). MINOXIDIL™, a popular hair loss treatment, is thought to work, at least in part, by mimicking this growth factor. Similarly it has been noted that severe baldness is strongly correlated with heart disease and even diabetes, so there appears to be some common etiology outside of the strictly androgen paradigm for pattern loss. There are likely other factors as well.
Another type of hair loss, alopecia areata, affects millions to some degree, though it is usually temporary. Alopecia areata is a non-scarring, inflammatory, hair loss disease. The factors that activate the onset of alopecia areata and the mechanisms of its development are not fully understood. Circumstantial evidence suggests alopecia areata is an autoimmune disease where cells of an individual's own immune system prevent hair follicles from producing hair fiber.
There are other types of hair loss as well. For example, localized hair loss can result from the build-up of scar tissue around surgical or trauma-induced wound sites. There remains a need in the art for an effective hair growth stimulant in the art for treating hair loss.